Normal Facial Nerves Research Articles

Better continuity of the facial nerve demonstrated in the temporal bone on three-dimensional T1-weighted imaging with volume isotropic turbo spin echo acquisition than that with fast field echo at 3.0 tesla MRI.

Three-dimensional (3D) T1-weighted imaging (T1WI) is used for evaluation of the facial nerve. The signal intensity of normal and pathological facial nerves has been well evaluated at both 1.5T and 3.0T MRI after gadolinium (Gd)-enhancement with various pulse sequences. However, the continuity of the facial nerve has not been evaluated on 3D-T1WI. This study aims to compare the continuity of the normal facial nerve in the temporal bone demonstrated on T1-weighted volume isotropic turbo spin echo acquisition (T1-VISTA), which is a spin-echo sequence, to that on T1-weighted fast field echo (T1-FFE), which is a gradient-echo sequence, at 3.0T MRI. Forty-four normal facial nerves in 22 healthy volunteers were imaged with both sequences using 3.0T MRI without Gd-enhancement. The facial nerves were evaluated visually by two neuroradiologists in four anatomical segments with a 3-point grading system of continuity. The continuity was assessed by summing the grades of the four segments as a total score. The grades at each segment and the total scores were compared statistically between the T1-VISTA and T1-FFE. The grades in all segments and the total score were significantly higher with T1-VISTA than those with T1-FFE. T1-VISTA was superior to demonstrate the facial nerve as a continuous anatomical structure in the temporal bone at 3.0T MRI.

Two Pathways Regulate Differential Expression of nAChRs Between the Orbicularis Oris and Gastrocnemius

BackgroundWe previously demonstrated differential expression of nicotinic acetylcholine receptors (nAChRs) in the facial nerve-innervated orbicularis oris and somatic nerve-innervated gastrocnemius, which contribute to different sensitivities to muscle relaxants. Furthermore, the orbicularis oris exhibits less sensitivity to muscle relaxants after facial nerve injury, which is also related to upregulation of nAChRs. Here, we explored the regulatory mechanism for the different expression patterns. Because the agrin/Lrp4/MuSK/rapsyn and neuregulin1/ErbB signaling pathways are indispensable for maintaining the expression of nAChRs, we examined the activity of these two signaling pathways in gastrocnemius and orbicularis oris innervated by normal or injured facial nerves. Materials and methodsA quantitative analysis of these two signaling pathways was realized by immunofluorescence, and immunoprecipitation was applied to detect the level of phosphorylated MuSK in the gastrocnemius and orbicularis oris innervated by normal or injured facial nerves in adult rats. ResultsErbB and the phosphorylated MuSK were expressed more in orbicularis oris than in gastrocnemius (P < 0.05). No significant difference was found in the expression of agrin/Lrp4/MuSK/rapsyn. After facial nerve injury, the level of agrin and the percentage of phosphorylated MuSK decreased significantly, although the expression levels of MuSK, rapsyn, and neuregulin1/ErbB were highly upregulated. ConclusionsDifferential expression of the neuregulin1/ErbB signaling pathway may account for the different expression patterns of nAChRs at the neuromuscular junctions of the orbicularis oris and gastrocnemius. Overexpression of MuSK and rapsyn may contribute to upregulation of nAChRs after facial nerve injury.

Estimation of Intraoperative Stimulation Threshold of the Facial Nerve in Patients Undergoing Microvascular Decompression.

Introduction Facial weakness can result from surgical manipulation of the facial nerve. Intraoperative neuromonitoring reduces functional impairment but no clear guidelines exist regarding interpretation of intraoperative electrophysiological results. Most studies describe subjects with facial nerves encumbered by tumors or those with various grades of facial nerve weakness. We sought to obtain the neurophysiological parameters and stimulation threshold following intraoperative facial nerve triggered electromyography (t-EMG) stimulation during microvascular decompression for trigeminal neuralgia to characterize the response of normal facial nerves via t-EMG. Methods Facial nerve t-EMG stimulation was performed in seven patients undergoing microvascular decompression for trigeminal neuralgia. Using constant current stimulation, single stimulation pulses of 0.025 to 0.2 mA intensity were applied to the proximal facial nerve. Compound muscle action potentials, duration to onset, and termination of t-EMG responses were recorded for the orbicularis oculi and mentalis muscles. Patients were evaluated for facial weakness following the surgical procedure. Results Quantifiable t-EMG responses were generated in response to all tested stimulation currents of 0.025, 0.05, 0.1, and 0.2 mA in both muscles, indicating effective nerve conduction. No patients developed facial weakness postoperatively. Conclusions The presence of t-EMG amplitudes in response to 0.025 mA suggests that facial nerve conduction can take place at lower stimulation intensities than previously reported in patients with tumor burden. Proximal facial nerve stimulation that yields responses with thresholds less than 0.05 mA may be a preferred reference baseline for surgical procedures within the cerebellopontine angle to prevent iatrogenic injury.

Differences in sensitivity to rocuronium among orbicularis oris muscles innervated by normal or damaged facial nerves and gastrocnemius muscle innervated by somatic nerve in rats

To evaluate mechanisms of discrepant responses to the nondepolarizing muscle relaxant rocuronium among normal and injured facial nerve-innervated orbicularis oris and tibial nerve-innervated gastrocnemius, and to provide information for the proper use of muscle relaxants to balance evoked electromyography (EEMG) monitoring and immobility in general anesthesia. Randomized controlled study. Right-sided facial nerve injury was induced by crush axotomy in 18 Sprague-Dawley rats. At different rocuronium concentrations, muscular tension amplitude (MTA) was determined in vitro for normal and injured facial nerve-innervated orbicularis oris and gastrocnemius; the number of unsaturated acetylcholine receptors (AChRs) at end plates was determined by (125) I-α-bungarotoxin staining followed with gamma spectroscopy. The morphological composition of muscle fibers was determined by histological examination. Following rocuronium incubation, the percentage of MTA inhibition (MTAI%) of gastrocnemius was significantly higher than the corresponding values of orbicularis oris (P < .05), and the degree of saturation of AChR in gastrocnemius was significantly greater than that in orbicularis oris (P < .05). The baseline MTA and AChR density of injured-side orbicularis oris was significantly smaller than those of the normal side, whereas no significant difference was found regarding MTAI% and the degree of AChR saturation between the normal and injured side. The affinity of AChR at end plates and different number of AChR per unit fiber cross-sectional area may be the mechanisms for differential sensitivities to neuromuscular blockers between facial nerve-innervated muscles and somatic nerve-innervated muscles. The lower EEMG responses in the impaired facial nerve-innervated muscles may result from the lower AChR density at end plates compared with the normal facial nerve-innervated muscles.

Enhancement Pattern of the Normal Facial Nerve on Three - Dimensional (3D) - Fluid Attenuated Inversion Recovery (FLAIR) Sequence at 3.0 T MR Units

Purpose : To compare the enhancement pattern of normal facial nerves on 3D-FLAIR and 3D-T1-FFE-F) sequences at 3.0 T MR units. Materials and Methods: We assessed 20 consecutive subjects without a history of facial nerve abnormalities who underwent temporal bone MRI with contrast enhancement between January 2008 and March 2009. Two neuroradiologists independently reviewed pre-/post-enhanced 3D-T1-FFE-FS and 3D-FLAIR images respectively with 2-week interval to assess the enhancement of normal facial nerves divided into five anatomical segments. The degree of enhancement in each segment was graded as none, mild or strong, and the results of 3D-FLAIR and 3D-T1-FFE-FS image sets were compared. Results: On 3D-FLAIR images, one of the two reviewers observed mild enhancement of the genu segment in two (10%) subjects. On 3D-T1-FFE-FS images, at least one segment of the facial nerve was enhanced in 13 (65%) subjects. At least one reviewer found that 17 of the 100 segments showed enhancement on 3D-T1-FFE-FS images, with the mastoid segment being the most commonly enhanced. Interobserver agreement on 3D-T1-FFE-FS images was good for enhancement of the normal facial nerve (= 0.589). Conclusion: In contrast to 3D-T1-FFE-FS, normal facial nerve segments rarely showed enhancement on 3D-FLAIR images.

Enhancement pattern of the normal facial nerve at 3.0 T temporal MRI.

The purpose of this study was to evaluate the enhancement pattern of the normal facial nerve at 3.0 T temporal MRI. We reviewed the medical records of 20 patients and evaluated 40 clinically normal facial nerves demonstrated by 3.0 T temporal MRI. The grade of enhancement of the facial nerve was visually scaled from 0 to 3. The patients comprised 11 men and 9 women, and the mean age was 39.7 years. The reasons for the MRI were sudden hearing loss (11 patients), Méniàre's disease (6) and tinnitus (7). Temporal MR scans were obtained by fluid-attenuated inversion-recovery (FLAIR) and diffusion-weighted imaging of the brain; three-dimensional (3D) fast imaging employing steady-state acquisition (FIESTA) images of the temporal bone with a 0.77 mm thickness, and pre-contrast and contrast-enhanced 3D spoiled gradient record acquisition in the steady state (SPGR) of the temporal bone with a 1 mm thickness, were obtained with 3.0 T MR scanning. 40 nerves (100%) were visibly enhanced along at least one segment of the facial nerve. The enhanced segments included the geniculate ganglion (77.5%), tympanic segment (37.5%) and mastoid segment (100%). Even the facial nerve in the internal auditory canal (15%) and labyrinthine segments (5%) showed mild enhancement. The use of high-resolution, high signal-to-noise ratio (with 3 T MRI), thin-section contrast-enhanced 3D SPGR sequences showed enhancement of the normal facial nerve along the whole course of the nerve; however, only mild enhancement was observed in areas associated with acute neuritis, namely the canalicular and labyrinthine segment.

A Correlation Study of Endoneurial Fluid Pressure and Electroneurography of the Facial Nerve

Objective: The relationship between endoneurial fluid pressure (EFP) and electroneurography (ENoG) of the facial nerve was studied in order to evaluate the pathophysilogical basis of ENoG to serve as the criteria for decompression of the facial nerve. Methods: While the values of ENoG were recorded by an instrument for physiology on the normal and crushed facial nerves of guinea pigs, EFPs were measured at the same time by a servo-nulling micropipette system. After the elevated EFP was measured, the facial nerves were removed and then fixed properly for examination under the light and electron microscope in order to determine the differences from various periods after injury. Results: With the change of EFP in the facial nerve during the period from day 3 to the third week after crushed injury, the percentage of degenerated facial nerve fiber increased. There was a positive correlation between ENoG and EFP. The coefficient was 0.88 and 0.51 in the second and third week after crushed injury, respectively. Extensive edema in endoneurial and perivascular spaces of the facial nerve could be found at the early stage of injury, while proliferation of numerous Schwann cells appeared at the later stage. Conclusion: The change of ENoG could reflect the value of EFP relatively within 3 weeks after crushed injury. Our data indicate that ENoG could be useful to evaluate the pathogenesis underlying facial palsy.

Vascular permeability to fluorescent substance in human cranial nerves.

It has recently been reported that in the facial canal, the facial nerve shows enhancement on gadolinium-enhanced magnetic resonance imaging in patients with clinically normal facial nerves. However, the mechanism of this enhancement has not yet been sufficiently clarified. The present study investigated the permeability of blood vessels in human cranial nerves that were obtained from surgically treated patients. The patients received an intravenous injection of sodium fluorescein 45 minutes before nerve resection. For histologic observation, the nerves were removed and frozen at -70 degrees C, and the sections were then cut at 4-microm thickness with a freezing microtome. The localization of the tracers was examined with a fluorescence microscope. Fluorescence was observed in the external nerve sheath and slightly in the endoneurium of these nerves, but was not observed within nerve fibers. These findings indicate that the vascular barrier in human peripheral nerves is incomplete.

Experimental Study on Facial Nerve Regeneration With or Without Geniculate Ganglionectomy

To investigate regeneration of the distal facial nerve following nerve grafting within the tympanic segment with geniculate ganglion preservation or dissection. Randomized controlled trial. Twenty-three adult New Zealand albino rabbits were used in this study. A 2-mm tympanic segment of the facial nerve was removed, and the greater auricular nerve was harvested for grafting in all animals. In group 1 (10 rabbits), the geniculate ganglion was preserved. In group 2 (13 rabbits), the geniculate ganglion was dissected. Mastoidal and extratemporal segments of the facial nerve were harvested 3 months postoperatively for histological examination by electron microscopy. The number of myelinated axons in normal facial nerves was 1819.6 +/- 535.6. In group 1, the number of myelinated axons was 123.6 +/- 31.1, and, compared with normal facial nerves, the diameter of the regenerative axons was decreased and the sheath thickness in the regenerative fiber was diminished. In group 2, the number of myelinated axons was 515.1 +/- 103.1, while the myelin sheath thickness was proportionate to axon diameter. (Data are given as mean +/- SD.) Geniculate ganglionectomy may improve motor axon regeneration.

Involvement of nitric oxide synthase in the physiology and pathophysiology of facial nerve function and dysfunction.

To date few reports have discussed the presence and function of nitric oxide (NO) in structures of the facial nerve. We performed nicotinamide adenine dinucleotide phosphate (NADPH-d)-diaphorase-histochemistry and immunohistochemistry on the intratemporal portion of the facial nerve, including the geniculate ganglion, of guinea pigs using specific antibodies to the three known isoforms of NO synthase and soluble guanylyl-cyclase (sGC). Normal facial nerves were compared to those treated intratympanically with bacterial lipopolysaccharides (LPS) and tumor necrosis factor-alpha (TNF-alpha). Both constitutive NOS isoforms and sGC could be detected in the bipolar ganglion cells of normal animals, while the inducible isoform (iNOS or NOS II) was not found. Endothelial NOS (NOS III) and sGC were present in blood vessels and were predominantly found in the perineurial sheath and less in the endoneurium. sGC could be detected in all fibers in a cross section of the facial nerve. LPS and TNF treatment led to the detection of iNOS in the perikaryia of the geniculate ganglion and the perineural sheath. These findings imply that NO may be involved in neurotransmission at least in the visceroafferent system. NO regulates vascular tone of nutrient blood vessels in the perineural sheath and endoneurium. The presence of sGC indicates that NO acts via its second messenger cGMP. NOS II expression may be a contributing factor to facial nerve palsy via two different mechanisms: NOS II-generated NO may lead to an overstimulation of the visceroefferent nerve fibers and motor fibers of the facial nerve. Dysregulation in facial nerve blood vessels could lead to edema and elevated pressure on the nerve within its osseous canal.

MR Findings of Facial Nerve on Oblique Sagittal MRI Using TMJ Surface Coil: Normal vs Peripheral Facial Nerve Palsy

Purpose: To evaluate the findings of normal facial nerve, as seen on oblique sagittal MRI using a TMJ (temporomandibular joint) surface coil, and then to evaluate abnormal findings of peripheral facial nerve palsy. Materials and Methods: We retrospectively reviewed the MR findings of 20 patients with peripheral facial palsy and 50 normal facial nerves of 36 patients without facial palsy. All underwent oblique sagittal MRI using a TMJ surface coil. We analyzed the course, signal intensity, thickness, location, and degree of enhancement of the facial nerve. According to the angle made by the proximal parotid segment on the axis of the mastoid segment, course was classified as anterior angulation (obtuse and acute, or buckling), straight and posterior angulation. Results: Among 50 normal facial nerves, 24 (48%) were straight, and 23 (46%) demonstrated anterior angulation; 34 (68%) showed iso signal intensity on T1WI. In the group of patients, course on the affected side was either straight (40%) or showed anterior angulation (55%), and signal intensity in 80% of cases was isointense. These findings were similar to those in the normal group, but in patients with post-traumatic or post-operative facial palsy, buckling, of course, appeared. In 12 of 18 facial palsy cases (66.6%) in which contrast materials were administered, a normal facial nerve of the opposite facial canal showed mild enhancement on more than one segment, but on the affected side the facial nerve showed diffuse enhancement in all 14 patients with acute facial palsy. Eleven of these (79%) showed fair or marked enhancement on more than one segment, and in 12 (86%), mild enhancement of the proximal parotid segment was noted. Four of six chronic facial palsy cases (66.6%) showed atrophy of the facial nerve. Conclusion: When oblique sagittal MR images are obtained using a TMJ surface coil, enhancement of the proximal parotid segment of the facial nerve and fair or marked enhancement of at least one segment within the facial canal always suggests pathology of the facial nerve. The use of this modality, together with the coil, is, therefore, an effective complementary technique for the evaluation of a facial nerve.

Contrast enhancement of the facial nerve on MRI: normal or pathological?

We prospectively analysed the normal contrast-enhanced MRI features of the facial nerve and determined criteria for pathological contrast enhancement. We studied 31 patients with clinically normal facial nerves with T1-weighted images before and after contrast medium. The intensity, thickness and right-left symmetry of enhancement were assessed in each segment and correlated with MRI features observed in abnormal facial nerves. Enhancement along at least one segment of the facial nerve was seen in 98% of cases, but only within the facial canal: labyrinthine segment: 78.2%; geniculate ganglion: 96.9%; tympanic: 88.4%; mastoid: 66.6%. Marked (+2) to intense (+3) enhancement was seen in the labyrinthine segment in 17.4%, the geniculate ganglion in 36.3%, and the tympanic (25.6%) and mastoid (7.1%) segments, whereas intense enhancement was only seen in the geniculate ganglion (6%) and the tympanic segment (11.6%). A right-left asymmetry was noted in 69% of cases. No correlation was found between enhancement and the thickness of the nerve. No enhancement of the eighth nerve was seen. We suggest three criteria for pathological enhancement: enhancement outside the facial canal; extension of enhancement to the eighth nerve; and intense enhancement in the labyrinthine and/or mastoid segments.

MRI of the facial nerve in idiopathic facial palsy.

The purpose of this prospective study was to define the enhancement pattern of the facial nerve in idiopathic facial paralysis (Bell's palsy) on magnetic resonance (MR) imaging with routine doses of gadolinium-DTPA (0.1 mmol/kg). Using 0.5T imager, 24 patients were examined with a mean interval time of 13.7 days between the onset of symptoms and the MR examination. Contralateral asymptomatic facial nerves constituted the control group and five of the normal facial nerves (20.8%) showed enhancement confined to the geniculate ganglion. Hence, contrast enhancement limited to the geniculate ganglion in the abnormal facial nerve (3 of 24) was referred to as equivocal. Not encountered in any of the normal facial nerves, enhancement of other segments alone or associated with geniculate ganglion enhancement was considered to be abnormal and noted in 70.8% of the symptomatic facial nerves. The most frequently enhancing segments were the geniculate ganglion and the distal intracanalicular segment.

MRI enhancement of the facial nerve with Gd-DTPA--first report--experimental study on the enhancement mechanism used in viewing vascular permeability of the facial nerve

Although there have recently been numerous reports of enhanced MRI in patients with facial palsy, the mechanism of enhancement remains largely unknown. In the present study, animal models with experimentally induced facial paralysis were prepared, and the vascular permeabilities of normal and damaged facial nerves were assessed using Evans blue albumin (EBA) as a tracer. The Gd-DTPA contents in normal and compressively damaged facial nerves were also investigated. The following results were obtained: 1. In the normal intratemporal facial nerve, EBA remained in the vessels, and did not leak into the endoneurium. In contrast, vascular permeability was very high in the epineurium and the geniculate ganglion which showed leakage of large amounts of EBA from vessels. 2. At the site of compression in the damaged nerve, EBA leakage was also seen in the endoneurism, indicating accentuated vascular permeability. This accentuation of vascular permeability shifted toward the distal side. However, no EBA leakage was seen on the side proximal to the site of compression. 3. Significantly higher Gd-DTPA contents were obtained in the facial nerve on the paralytic side than in that on the normal side (p < 0.001). As for differences between the distal and proximal sides, the distal side had a significantly higher Gd-DTPA content (p < 0.01). Assessment of vascular permeability with EBA revealed accentuated vascular permeability on the side distal to the site of compression. These results showed the presence of a blood nerve barrier (BNB) in the facial nerve.(ABSTRACT TRUNCATED AT 250 WORDS)

Enhancement along the normal facial nerve in the facial canal: MR imaging and anatomic correlation.

Normal facial nerves are reported to show no enhancement at magnetic resonance (MR) imaging, in contradiction to the authors' clinical experience. To investigate this inconsistency, the authors searched MR imaging files and clinical records to find patients who underwent MR imaging of the temporal bone (at 1.5 T) before and after intravenous administration of gadopentetate dimeglumine and who had bilateral clinically normal facial nerves. When the MR images of 93 patients (186 facial nerves) were analyzed subjectively, 142 nerves (76%) were visibly enhanced along at least one segment of the facial nerve within the facial canal; the nerves of 64 of the 93 patients (69%) showed right-left asymmetry in enhancement, which was inhomogeneously distributed along each nerve. The facial nerve in the cerebellopontine angle cistern and in the internal auditory canal, as well as in the visualized proximal portion of the extracranial facial nerve, showed no enhancement. Comparison with reference anatomic sections showed that this enhancement pattern corresponded exactly to the topography of the circumneural facial arteriovenous plexus and should not necessarily be considered a sign of anatomic abnormality.

Gadolinium‐enhanced magnetic resonance imaging in facial nerve lesions

We present our 2-year experience with a contrast enhancement agent in magnetic resonance imaging (MRI) examining facial nerve pathology. Characteristics of the agent gadolinium diethylenetriamine pentaacetic acid are reviewed. The radiographic capability to differentiate pathologic vs. normal facial nerves based on enhancement and a change in signal intensity generated by the nerve is demonstrated. Experience with facial nerve disorders including Bell's palsy, facial nerve neuromas, a facial nerve graft site, postoperative facial paralysis, and traumatic facial paralysis is presented. The ability to image the facial nerve in Bell's palsy provides an entirely new means of examining this disorder, and its implications are discussed. The ability to enhance the paralyzed facial nerve in the temporal bone after posterior fossa surgery supports a previously held concept as to the pathophysiology of this problem.

Vestibular, facial, and oculomotor neuropathy in diabetes mellitus.

A diabetic patient experienced multiple neuropathies involving the oculomotor, facial, and vestibular nerves. Recovery of motor function was complete following the oculomotor and facial palsies. The vestibular paralyses were acute and severe and also followed by compensatory recovery. Temporal bone studies show normal facial nerves. There is partial degeneration of the vestibular nerves which is interpreted to represent the pathological sequela of acute diabetic vestibular neuritis.